ArticleClinical and translational medicine2022
The driver role of JAK-STAT signalling in cancer stemness capabilities leading to new therapeutic strategies for therapy- and castration-resistant prostate cancer.
Article in Clinical and translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 40 citations in OpenAlex.
- Cancer stem cell plasticity: mechanisms, immune microenvironment crosstalk, and therapeutic implications.Journal of hematology & oncology · 2026Review
- Article
- IGFBP3-SphK1/S1P Signaling Axis Drives Enzalutamide Resistance in Advanced Prostate Cancer.Molecular cancer therapeutics · 2026Article
- Game of clones: decipher lineage plasticity in hormone-driven cancers.Cellular and molecular life sciences : CMLS · 2026Review
- LUCAT1 promotes stemness in head and neck squamous cell carcinoma by sponging miR-128.Frontiers in oncology · 2026Article
- Circadian regulator REV-ERBα is a master regulator of tumor lineage plasticity and an effective therapeutic target.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Lineage plasticity and histological transformation: tumor histology as a spectrum.Cell research · 2025Review
- Dynamic Reprogramming of Immune-Related Signaling During Progression to Enzalutamide Resistance in Prostate Cancer.Cancers · 2025Article
- Article
- Gland- and cell-level heterogeneity in the prostate: A narrative review of related diseases.Current urology · 2025Article
- STAT1-mediated interferon signatures are associated with preclinical JAK inhibitor sensitivity in T-ALL.Blood · 2025Article
- PROX1 is an early driver of lineage plasticity in prostate cancer.The Journal of clinical investigation · 2025Article
- Review
- Comparative transcriptomics reveals a mixed basal, club, and hillock epithelial cell identity in castration-resistant prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- AGD1/USP10/METTL13 complexes enhance cancer stem cells proliferation and diminish the therapeutic effect of docetaxel via CD44 m6A modification in castration resistant prostate cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- JAK-STAT Signaling in Autoimmunity and Cancer.ImmunoTargets and therapy · 2025Review
- JAK/STAT signaling maintains an intermediate cell population during prostate basal cell fate determination.Nature genetics · 2024Article
- MicroRNAs as Promising Therapeutic Agents Against Prostate Cancer Resistant to Castration-Where Are We Now?Pharmaceutics · 2024Review
- Neuroendocrine transdifferentiation in human cancer: molecular mechanisms and therapeutic targets.MedComm · 2024Review
- Cellular senescence in metastatic prostate cancer: A therapeutic opportunity or challenge (Review).Molecular medicine reports · 2024Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundLineage plasticity in prostate cancer (PCa) has emerged as an important mechanism leading to the onset of therapy- and castration-resistant PCa (t-CRPC), which is closely associated with cancer stem cell (CSC) activity. This study is to identify critical driver(s) with mechanism of action and explore new targeting strategy.
methodsVarious PCa cell lines with different genetic manipulations were subjected to in vitro prostasphere assay, cell viability assay and in vivo stemness potential. In addition, bioinformatic analyses such as Ingenuity pathway and Gene Set Enrichment Analysis were carried out to determine clinical relevance. The in vivo anti-tumour activity of JAK or STAT1 inhibitors was examined in clinically relevant t-CRPC model.
resultsWe demonstrated the role of interferon-related signalling pathway in promoting PCa stemness, which correlated with significant elevation of interferon related DNA damage resistance signature genes in metastatic PCa. Inhibition of JAK-STAT1 signalling suppresses the in vitro and in vivo CSC capabilities. Mechanistically, IFIT5, a unique downstream effector of JAK-STAT1 pathway, can facilitate the acquisition of stemness properties in PCa by accelerating the turnover of specific microRNAs (such as miR-128 and -101) that can target several CSC genes (such as BMI1, NANOG, and SOX2). Consistently, knocking down IFIT5 in t-CRPC cell can significantly reduce in vitro prostasphere formation as well as decrease in vivo tumour initiating capability.
conclusionsThis study provides a critical role of STAT1-IFIT5 in the acquisition of PCSC and highlights clinical translation of JAK or STAT1 inhibitors to prevent the outgrowth of t-CRPC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.